To investigate the meaning of the mutation screening, prevalence, inheritance and the intervention or the prevention for the specific drugs in 10 families with non-syndrome hearing loss in Yunnan Province, China. To do a questionnaire about the cases of ten families with non-syndrome hearing loss and to draw a detailed matriarchal family tree detailed. Following that, the A1555G mutation-positive individuals were detected and confirmed using DNA extracting, PCR amplification and sequencing for family volunteer. There are 96 members have attended the blood collection in these ten families. Thirty-six of them had the normal hearing and 60 of them had the sensory neural hearing loss. However, 4 out of those had no A1555G point mutation, and 92 had A1555G point mutation (95.8%). While 7 of those were Heterogeneity, the rest were all homogeneous mutation. There were also 73 patients who had amino glycoside antibiotic medication history. However all the rest cases had a history of amino glycoside antibiotic medication were not clear yet. The proportion of patients with drug-induced deafness is high in Yunnan province and the mutation rate of mitochondrial DNA A1555G is also high. It is worthy to do DNA 12SrRNA A1555G mutation screening for drug intervention and prevention.
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Objective: To observe the change of congnitive function and the expression level of hippocampal insulin receptors (InsR) in 1 month and 3 months of diabetic rats, explore the effect of InsR on diabetic rats and investigate that whether insulin can be applied to prevent diabetic cognitive impairment. Methods: 36 healthy adult male SD (Sprague - Dawley) rats, weight 180-240 g, were divided into 3 groups randomly: diabetic group (n = 12), insulin treatment group (n = l2) and control group (re = 12), and then each group was divided into 2 groups equal in amount randomly: 1 month group and 3 months group. Diabetic group and insulin treatment group rats were induced by streptozotocin injection. Fixed time to measure blood glucose of all rats twice a week. Insulin treatment group rats were injected insulin daily, and we adjusted insulin dosage according to the blood glucose level to ensure blood glucose in normal range. All the rats underwent the test of Morris water maze in 1 month and 3 months. After the assessment on cognitive function of the 1 month and 3 months rats that experienced the Morris water maze experiment, the expression of InsR in brain were observed. Results: Compared with the control group, 1 month group of diabetic rats appeared cognitive impairment and their expression of InsR reduced, which has statistical difference (P < 0.05). Compared with 1 month diabetic group, the cognitive impairment of 3 months diabetic group was obviously aggravated and their expression of InsR reduced more significantly, which has statistical difference as well (P<0.05). 1 month group of insulin treatment rats with no significant cognitive impairment, and their expression of InsR reduced slightly. Compared with the control group, there are no difference. Compared with the 1 month diabetic group, which has statistical difference (P<0.05). 3 months group of insulin treatment rats appeared cognitive impairment and their expression of InsR reduced obviously. Compared with control group, which has statistical difference (P <0.05). Compared with 1 month group of insulin treatment rats, which has statistical difference as well (P <0. 05). Compared with 3 months group of diabetic rats, there are no statistical difference. Conclusion: Diabetic cognitive impairment is closely related to InsR, the reduced InsR expression may contribute to diabetic cognitive impairment. Early intervention of insulin has protective effect on the brain, then delay cognitive impairment. However, as the extension of the duration, the insulin treatment group rats still show cognitive impairment, which suggests that long - term application of insulin can not prevent the occurrence of cognitive impairment. Mechanisms need to be further explored.
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